Blast related traumatic brain injury (bTBI) is a frequent outcome of exposure to explosive device detonation. During Operation Iraqi Freedom and Operation Enduring Freedom in Afghanistan, improvised explosive devices (IED), vehicle borne IED and improvised rocket assisted mortars have become the preferred weapons used against American troops. Over 300,000 US military personnel are documented to have suffered bTBI due to IED blast exposures over the last 10 years of war. According to the Defense and Veterans Brain Injury Center, more than 50% of injuries sustained during the conflicts in Iraq and Afghanistan are the result of explosives including bombs, grenades, land mines, mortar/artillery shells and IEDs Since 2006, blasts have been the most common cause of injury among American solders treated at Walter Reed Army Medical Center.
In addition to the destroyed lives and families, researchers estimate that the cost of treating a solder with severe bTBI is between $600,000 and $5,000,000 over his or her lifetime.
TBI (traumatic brain injury) from explosive blasts are poorly understood due to the near impossibility of doing human research on the mechanisms of causation. While animal research has been done, the animal models have not been validated to correlate with human injuries. After the blast, the noninvasive methods of detecting focal and often subtle brain injuries in injured soldiers are not adequately reliable or sensitive. Finally, further confusion is added because there are multiple causative mechanisms that each result in different brain injuries which all interact and add up to the total injury. Virtually all of the research to date has focused on defining the injuries that add up to the TBI, defining the mechanisms of injury and possible treatments after the injury. The instant inventors are not aware of any viable suggestions for preventing or reducing TBI due to explosive blasts.
It is currently thought that there are three basic mechanisms of TBI from explosive blasts:
Primary blast injuries are caused by blast overpressure waves or shock waves. High-order explosives produce a supersonic shock wave of high-pressure air lasting a few milliseconds. The excess barometric pressure can reach up to 100 pounds per square inch (PSI) traveling at a velocity of 1500 mph (an overpressure of 60-80 PSI is considered potentially lethal). To put this in perspective, blasts and blast pressure waves are obviously a regular part of combat in one degree or another. For example, a large bore rifle or pistol produces sound pressure levels of 170-175 dB, which is approximately equal to 1 PSI of air pressure. A howitzer crew may be subjected to blast pressures of 5 PSI each time they shoot their gun.
The overpressure waves cause the most damage to air-filled organs such as the ear, lung and gastrointestinal tract. Since the brain is protected by a non-compressible, rigid skull and does not have compressible air within the skull, most investigators currently believe that the blast overpressure waves are not significant direct contributors to blast induced TBI.
However, there is good evidence that blast overpressure waves compressing the chest indirectly contribute to TBI. A number of animal studies have shown that the rapid and massive compression of the chest forces high-pressure blood into the non-compliant cranial vault. The result is a momentarily huge increase in the intracranial pressure, known as hydrostatic or hydraulic shock. Post mortem animal studies of this phenomenon show wide-spread leaking from blood vessels within the brain, a phenomenon that is well known to cause brain damage much like multiple small hemorrhagic strokes.
Secondary blast injuries are caused by fragmentation and other objects propelled by the explosion causing penetrating injuries to the head.
Tertiary blast injuries are caused by the high velocity “blast wind” that follows the shock wave. The blast wind first expands out from the explosion at up to 330 mph and then may reverse direction when the air around the explosion gets sucked back to fill the vacuum created by the blast or if the blast wave is reflected off of a solid object like a wall. These high velocity blast winds cause the head and extremities to move violently first in one direction and then in the opposite direction. This movement is virtually identical to the violent movement seen in whiplash injuries from high-speed motor vehicle crashes. The TBI from this violent angular acceleration/deceleration of the head whipping back and forth faster than the body (which has a higher mass and is, therefore, harder to accelerate), results in the coup/countercoup brain injuries seen in both humans and animal models of blast injuries, as well as neck injuries.
Animal research shows that mouse brains are significantly protected when the head of the animal is stabilized so that it cannot be whipped back and forth by the blast wind.
Tertiary blast injuries may also occur when the blast winds cause the soldier to be thrown onto a solid object such as a wall or the ground. A severe impact to the head of the soldier can obviously contribute to the total bTBI.
It is apparent that there are several tertiary mechanisms of blast injury, each of which contribute in varying degrees to the total bTBI caused by the explosion. bTBI is a complex brain injury caused by multifactorial assaults emanating from the blast. Each of these multifactorial assaults are affected by multiple factors such as: size of the explosion, distance from the explosion, orientation of the person to the explosion, use of body armor and helmets, proximity to reflecting objects such as walls or vehicles and the body part that hits the ground or wall first, to name a few. The resulting bTBI is the summation of all of these focal and unpredictable injuries.
In the case where the blast itself is not preventable or avoidable, protection measures against the blast may be useful. Current research suggests that the blast overpressure wave itself may not be a major contributor to the bTBI (primary blast injury).
Finally, the secondary blast injuries caused by penetrating fragmentation injuries may not be preventable or avoidable and are beyond the scope of this patent. Therefore, if preventive measures are going to be useful, they must be focused on preventing the tertiary blast injuries.
Critical to understanding this invention is understanding that there is an obligatory time delay between the nearly instantaneous arrival of the blast wave and the arrival of the slower moving blast wind, which is the cause of the tertiary blast injuries. There is an additional time delay between the arrival of the blast wind and the resulting angular acceleration and movement of the head relative to the heavier, slower accelerating body. Then there is an additional time delay between the acceleration of the body (and head) through the air and the rapid deceleration of that head and body as it impacts the ground or other hard object. Finally, the hydrostatic shock wave to the brain is also delayed because the chest must first be compressed, forcing the blood out of the chest under high pressure into the arteries and veins of the neck and then into the skull—all of which takes time.
We will assume a worst case, but still possibly survivable scenario of an explosion occurring 10 ft. from the soldier and the resulting blast wind velocity of 300 mph. In this case there is a 0.023 second or 23 millisecond (msec.) time delay between the arrival of the blast wave and the arrival of the blast wind. It is also reasonable to assume that the acceleration resulting in movement of the head relative to the body and the movement of the body relative to the ground will add an additional 20-100 msec. in delay. Therefore, in the worst case scenario, there is a minimum of a 43 msec. time delay between the arrival of the blast wave and the onset of the tertiary blast injuries. Obviously, the time delay is greater if the explosion is further from the soldier or if the injury is from being thrown to the ground. It is reasonable to estimate that the tertiary blast injuries occur between 43 msec. and 200 msec. after the arrival of the blast wave.
It is logical to assume that if any of the contributing mechanisms of tertiary blast injury can be reduced or eliminated, the resulting focal injuries should be reduced and the resulting sum total bTBI should also be reduced. The 43 msec. to 200 msec. time delay gives a brief opportunity to intervene and possibly mitigate the damaging effects of some or all of the tertiary mechanisms of injury due to the blast wind that lead to bTBI following an explosion. There is also an opportunity to intervene and possibly mitigate the damaging effects of some or all of the indirect primary mechanisms of bTBI injury due to the blast overpressure wave producing hydraulic shock by occluding the major blood vessels between the chest and the brain, preventing the high-pressure blood from reaching the brain.
A wide variety of inflatable protective devices have been disclosed over many years. These have been designed to protect the head, neck and/or body of persons who are falling or crashing (bicycles, motorcycles, automobiles, racecars and pilots). Some examples include: Alstin discloses a helmet for a bicycle rider that inflates during a crash in U.S. Pat. No. 8,402,568. Ommaya in U.S. Pat. No. 3,765,412; Martin in U.S. Pat. No. 5,133,084; Green in U.S. Pat. No. 5,402,535; Archer in U.S. Pat. No. 5,313,670 all disclose inflatable neck collars for protecting automobile drivers, racecar drivers, motorcyclists and pilots from neck injuries during crashes. Colombo in U.S. Pat. No. 7,370,370 and Pusic in U.S. Pat. No. 5,091,992 disclose inflatable suits that inflate during a motorcycle crash. Buchman in U.S. Pat. No. 7,150,048 discloses a variety of inflatable suits that inflate during a fall for protection of the elderly. All of these prior art devices are variations of airbag technologies that have been developed for automotive safety over the past 50 years.
All of the cited prior art as well as the automobile airbag technologies rely on the detection of rapid deceleration, acceleration, angular acceleration or changes in attitude to determine if a crash or fall is in progress and then to trigger the safety device. Accelerometers and gyroscopes are used to detect the acceleration/deceleration and then sophisticated algorithms analyze the input data to determine whether or not the detected acceleration is a crash or fall that requires deployment of the airbag.